Government-Owned Inventions; Availability for Licensing, 29334-29336 [05-10065]

Download as PDF 29334 Federal Register / Vol. 70, No. 97 / Friday, May 20, 2005 / Notices than by recombination in mammalian cells. 2. It can be used to produce recombinant vaccinia viruses for gene expression. 3. It can be used for the production of modified vaccinia viruses that have improved safety or immunogenicity. Advantages of the VAC–BAC shuttle system: 1. VAC–BACs are clonally purified from bacterial colonies before virus reconstitution in mammalian cells. 2. Manipulation of DNA is much simpler and faster in bacteria than in mammalian cells. 3. Modified genomes can be characterized prior to virus reconstitution. 4. Only virus with modified genomes will be produced so that virus plaque isolations are not needed. 5. Generation of a stock of virus from a VAC–BAC is accomplished within a week rather than many weeks. 6. Multiple viruses can be generated at the same time since plaque purification is unnecessary. References: 1. Domi, A., and B. Moss. 2002. Cloning the vaccinia virus genome as a bacterial artificial chromosome in Escherichia coli and recovery of infectious virus in mammalian cells. Proc. Natl. Acad. Sci. USA 99:12415– 12420. 2. Domi, A., and B. Moss. 2005. Engineering of a vaccinia virus bacterial artificial chromosome in Escherichia coli by bacteriophage lambda-based recombination. Nature Methods 2:95– 97. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Dated: May 12, 2005. Steven M. Ferguson, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. 05–10064 Filed 5–19–05; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health Government-Owned Inventions; Availability for Licensing National Institutes of Health, Public Health Service, DHHS. ACTION: Notice. AGENCY: SUMMARY: The inventions listed below are owned by an agency of the U.S. VerDate jul<14>2003 20:07 May 19, 2005 Jkt 205001 Government and are available for licensing in the U.S. in accordance with 35 U.S.C. 207 to achieve expeditious commercialization of results of federally-funded research and development. Foreign patent applications are filed on selected inventions to extend market coverage for companies and may also be available for licensing. ADDRESSES: Licensing information and copies of the U.S. patent applications listed below may be obtained by writing to the indicated licensing contact at the Office of Technology Transfer, National Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, Maryland 20852–3804; telephone: 301/ 496–7057; fax: 301/402–0220. A signed Confidential Disclosure Agreement will be required to receive copies of the patent applications. DU145 Camptothecin (CPT)-Resistant Cell Line Dr. Yves Pommier (NCI) DHHS Reference No. E–159–2005/0— Research Tool Licensing Contact: John Stansberry; 301/ 435–5236; stansbej@mail.nih.gov Drug resistance is a major limitation of chemotherapy. Understanding how drug resistance develops may lead to more effective treatments. This invention describes the DU145 Camptothecin (CPT)-resistant prostate cancer cell line that can be used to study mechanisms of drug resistance. For more details see Pommier et al., Cancer Research 61, 1964–1969, March 1, 2001. Mammary Gland Differentiation by 2Methoxyestradiol Jeffrey E. Green et al. (NCI) DHHS Ref. No. E–069–2005/0–US–01 Licensing Contact: Thomas P. Clouse; 301/435–4076; clouset@mail.nih.gov This invention is based on the discovery that administration of 2Methoxyestradiol (2-ME2) to female mice at various developmental stages will result in the differentiation of mammary epithelial cells to form rudimentary alveolar structures and to produce milk proteins. This effect has also been demonstrated in an in vitro experimental system. Since 2-ME2 is highly expressed during late stages of human pregnancy and pregnancy is known to reduce the risk of human bresat cancer, possibly due to differentiating effects on the mammary gland, 2ME2 may be developed into a preventive agent against breast cancer in women. Additionally, 2-ME2 may be useful in augmenting mammary gland differentiation and milk production PO 00000 Frm 00066 Fmt 4703 Sfmt 4703 under circumstances where normal differentiation is compromised. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Methods for Detecting Progression of Low Grade Cervical Dysplasia Thomas Ried et al. (NCI) DHHS Reference No. E–041–2005/0– US–01 Licensing Contact: Thomas P. Clouse; 301/435–4076; clouset@mail.nih.gov This invention describes a test that can be applied to Pap smears to differentiate low-grade dysplastic lesions that are likely to progress to higher-grade dysplasia and cervical cancer from those that are likely to regress. The differentiating factor is the presence of genetic gain on the long arm of chromosome 3. The inventors have shown that low grade Pap smears that progress already exhibit extra copies of 3q, while those that do not show the 3q gain spontaneously regress. Around 10–15% of the 3 million Pap smears with low-grade dysplasia each year in the United States progress to higher grade lesions. Currently, HPV testing is used to stratify these low grade disease Pap smears, but as the majority of these Pap smears are already HPV infected, the test has very low specificity. The instant 3q test, which targets the human telomerase gene, TERC, is a significant improvement in sensitivity and specificity over the current methods used for the detection of progressing versus regressing lesions. Antibodies to Rheb, a Ras-Related Protein Geoffrey J. Clark and Michele Vos (NCI) DHHS Reference No. E–351–2004— Research Tool. Licensing Contact: Mojdeh Bahar; 301/ 435–2950; baharm@mail.nih.gov The invention relates to polyclonal antibodies that recognize the protein Rheb, a key player in protein biosynthesis. Rheb is a small GTPbinding protein that is structurally related to the oncoprotein Ras, but Rheb does not activate the same pathways as Ras. Instead, Rheb binds to the tumor suppressor TSC2 (Tuberin) and causes activation of the S6 kinase in a TOR (Target of Rapamycin) dependent manner. Rheb likely plays roles in the response to insulin and the development of human tumors. Thus, the antibodies could provide useful reagents to investigate the functions of Rheb in these and other biological processes. E:\FR\FM\20MYN1.SGM 20MYN1 Federal Register / Vol. 70, No. 97 / Friday, May 20, 2005 / Notices In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. Methods of Reducing the Activity and Concentration of an Eph Receptor Tyrosine Kinase Jennifer Isaacs and Leonard Neckers (NCI) U.S. Provisional Application No. 60/ 591,986 filed 29 Jul 2004 (DHHS Reference No. E–245–2004/0–US–01) Licensing Contact: George Pipia; 301/ 435–5560; pipiag@mail.nih.gov The Eph receptors comprise a family of 14 members and as such, they carry out diverse functions, including embryonic patterning, migration, and the formation of neural networks. Recently, it was discovered that a subset of these proteins play an integral role in the formation of blood vessels, or angiogenesis, which is a process essential to tumor development. In fact, several of these proteins have the capacity to transform normal cells, when overexpressed. We have discovered that the HSP90 inhibitor 17Allylamino-17-demethoxygeldanamycin (17–AAG) effectively downregulates the level of several angiogenic Eph receptors and impairs their oncogenic signaling. This suggests that it maybe possible treat cancers overexpressing these oncogenes, by selectively inhibiting HSP90 with 17–AAG and its derivatives. Retinal Pigment Epithelial Cells Immortalized with TERT and Expressing the Adenoviral E1A Oncoprotein Karen Vousden et al. (NCI) DHHS Reference No. E–135–2004/0— Research Tool Licensing Contact: Thomas P. Clouse; 301/435–4076; clouset@mail.nih.gov This invention describes human retinal pigment epithelial cells immortalized with telomerase reverse transcriptase (TERT). Some of these cells express the adenoviral E1A oncoprotein, while others do not. The E1A expressing cells serve as a model for cancerous cells. Those that do not express E1A behave like normal cells. As such these immortalized cells can be used to compare the behavior of normal and cancer cells in vitro. Analogs of Thalidomide as Potential Angiogenesis Inhibitors William D. Figg, Erin Lepper (NCI) U.S. Provisional Application No. 60/ 486,515 filed 11 Jul 2003 (DHHS Reference No. E–272–2003/0–US–01); PCT Application No. PCT/US04/ VerDate jul<14>2003 20:07 May 19, 2005 Jkt 205001 22242 filed 09 Jul 2004 (DHHS Reference No. E–272–2003/0–PCT– 02) Licensing Contact: Jesse Kindra; 301/ 435–5559; kindraj@mail.nih.gov The present disclosure relates to antiangiogenesis compositions and methods, and particularly thalidomide analogs that actively inhibit angiogenesis in humans and animals. Angiogenesis is the formation of new blood vessels from pre-existing vessels. Angiogenesis is prominent in solid tumor formation and metastasis. A tumor requires formation of a network of blood vessels to sustain the nutrient and oxygen supply for continued growth. Some tumors in which angiogenesis is important include most solid tumors and benign tumors, such as acoustic neuroma, neurofibroma, trachoma, and pyogenic granulomas. Prevention of angiogenesis could halt the growth of these tumors and the resultant damage due to the presence of the tumor. The subject application discloses active thalidomide analogs that exhibit enhanced potency in the inhibition of undesirable angiogenesis, and methods for using these compounds to treat angiogenesis and solid tumors. In particular, the presently disclosed method provides for inhibiting unwanted angiogenesis in a human or animal by administering to the human or animal with the undesired angiogenesis a composition comprising an effective amount of the active thalidomide analogs. According to a more specific aspect, the method involves inhibiting angiogenesis by exposing a mass having the undesirable angiogenesis to an angiogenesis inhibiting amount of one or more compounds, or pharmaceutically acceptable salts of such compounds. Mycolactone and Related Compounds Pamela L. Small and Kathleen M. George (NIAID) U.S. Patent 6,680,055 issued 20 Jan 2004 (DHHS Reference No. E–199–1999/0– US–06) Licensing Contact: John Stansberry; 301/ 435–5236; stansbej@mail.nih.gov This application describes and claims novel pharmocoactive compounds which belong to the class of compounds known as polyketide macrolides. These compounds have been isolated from M. ulcerans the causative agent of buruli ulcers. Early work with these compounds suggests that the principle compound, mycolactone, or mixtures of mycolactone with other isolated polyketide macrolides or other agents may be useful in treating cancer or suppressing an inflammatory response. PO 00000 Frm 00067 Fmt 4703 Sfmt 4703 29335 In addition to the novel polyketide macrolide compounds the application also describes compositions derived from a non-virulent strain of M. ulcerans. These compositions may be useful in inducing an immune response (vaccines) which could be useful in providing subjects with resistance to the development of buruli ulcers. Antibodies against mycolactone are being developed. These antibodies could be used for diagnostic purposes. Some early publications which describe this work are KM George et al. Science 283(5403): 854–7 (Feb. 5, 1999) and KM George et al. Infect. Immun. 66(2): 587–93 (Feb. 1998). More recently, novel mycolactones have been isolated and characterized from Australian isolates of M. ulcerans (Judd et al. Organic Lett. 6: 4901–4904 (2004)) as well as from the frog pathogen M. liflandii (Mve-Obiang, A. et al. Infect. Immun. (In Press)). Spatial and Temporal Control of Gene Expression Using a Heat Shock Protein Promoter in Combination with Local Heat Chrit T. Moonen (ORS) U.S. Patent Application No. 10/864,102 filed 09 Jun 2004, claiming priority to 15 Aug 1996 (DHHS Reference No. E– 235–1995/0–US–09); Foreign rights available Licensing Contact: George Pipia; 301/ 435–5560; pipiag@mail.nih.gov In many instances, it is desirable to express exogenous genes only in certain tissues, and/or at will at certain times, and/or only to a certain degree. However, current gene transfer and exogenous gene expression protocols do not provide adequate means of simultaneously controlling which cells in a heterogeneous population are transformed and when, where, and to what degree the transferred genes are expressed. The invention provides methods for using local heat to control gene expression. The heat shock protein (hsp) gene promoter is recombined with a selected therapeutic gene and expressed in selected cells. Local controlled heating is used to activate the hsp promoter, for example by using focused ultrasound controlled by MRI. In addition to licensing, the technology is available for further development through collaborative research opportunities with the inventors. E:\FR\FM\20MYN1.SGM 20MYN1 29336 Federal Register / Vol. 70, No. 97 / Friday, May 20, 2005 / Notices Dated: May 11, 2005. Steven M. Ferguson, Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health. [FR Doc. 05–10065 Filed 5–19–05; 8:45 am] BILLING CODE 4140–01–P DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Cancer Institute; Notice of Meeting Pursuant to section 10(a) of the Federal Advisory Committee Act, as amended (5 U.S.C. Appendix 2), notice is hereby given of a meeting of the National Cancer Institute Board of Scientific Advisors. The meeting will be open to the public, with attendance limited to space available. Individuals who plan to attend and need special assistance, such as sign language interpretation or other reasonable accommodations, should notify the Contact Person listed below in advance of the meeting. Name of Committee: National Cancer Institute Board of Scientific Advisors. Date: June 27–28, 2005. Time: June 27, 2005, 8 a.m. to 6 p.m. Agenda: Director’s Report; Ongoing and New Business; Reports of Program Review Group(s); and Budget Presentation; Reports of Special Initiatives; RFA and RFP Concept Review; and Scientific Presentations. Place: National Institutes of Health, Building 31, C Wing, 6 Floor, Conference Rm. 10, 9000 Rockville Pike, Bethesda, MD 20892. Time: June 28, 2005, 8:30 a.m. to 1 p.m. Agenda: Ongoing and New Business; Reports of Program Review Group(s); and Budget Presentation; Reports of Special Initiatives; RFA and RFP Concept Review; and Scientific Presentations. Place: National Institutes of Health, Building 31, C Wing, 6 Floor, Conference Rm. 10, 9000 Rockville Pike, Bethesda, MD 20892. Contact Person: Paulette S. Gray, PhD, Executive Secretary, Division of Extramural Activities, National Cancer Institute, National Institutes of Health, 6116 Executive Boulevard, 8th Floor, Rm. 8001, Bethesda, MD 20892, (301) 496–5147. Any interested person may file written comments with the committee by forwarding the statement to the Contact Person listed on this notice. The statement should include the name, address, telephone number and when applicable, the business or professional affiliation of the interested person. In the interest of security, NIH has instituted stringent procedures for entrance into the building by non-government employees. Persons without a government I.D. will need to show a photo I.D. and signin at the security desk upon entering the building. VerDate jul<14>2003 20:07 May 19, 2005 Jkt 205001 Information is also available on the Institute’s/Center’s home page: https:// deainfo.nci.nih.gov/advisory/bsa.htm, where an agenda any any additional information for the meeting will be posted when available. (Catalogue of Federal Domestic Assistance Program Nos. 93.392, Cancer Construction; 93.393, Cancer Cause and Prevention Research; 93.394, Cancer Detection and Diagnosis Research; 93.395, Cancer Treatment Research; 93.396, Cancer Biology Research; 93.397, Cancer Centers Support; 93.398, Cancer Research Manpower; 93.399, Cancer Control, National Institutes of Health, HHS.) Dated: May 12, 2005. LaVerne Y. Stringfield, Director, Office of Federal Advisory Committee Policy. [FR Doc. 05–10070 Filed 5–19–05; 8:45 am] BILLING CODE 4140–01–M DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Cancer Institute; Notice of Closed Meeting Pursuant to section 10(d) of the Federal Advisory Committee Act, as amended (5 U.S.C. Appendix 2) notice is hereby given of the following meeting. The meeting will be closed to the public in accordance with theprovisions set forth in sections 552b(c)(4) and 552b(c)(6), Title 5 U.S.C., as amended. The grant applications and the discussions could disclose confidential trade secrets or commercial property such as patentable material, and personal information concerning individuals associated with the grant applications, the disclosure of which would constitute a clearly unwarranted invasion of personal privacy. Name of Committee: National Cancer Institute Initial Review Group, Subcommittee F—Manpower & Training. Date: June 14–15, 2005. Time: 8 a.m. to 5 p.m. Agenda: To review and evaluate grant applications. Place: Wyndham City Center Hotel, 1143 New Hampshire Ave., NW., Washington, DC 20037. Contact Person: Lynn M. Amende, PhD, Scientific Review Administrator, Resources and Training Review Branch, Division of Extramural Activities, National Cancer Institute, 6116 Executive Blvd., Room 8105, Bethesda, MD 20892, 301–451–4759, amendel@mail.nih.gov. (Catalogue of Federal Domestic Assistance Program Nos. 93.392, Cancer Construction; 93.393, Cancer Cause and Prevention Research; 93.394, Cancer Detection and Diagnosis Research; 93.395, Cancer Treatment Research; 93.396, Cancer Biology PO 00000 Frm 00068 Fmt 4703 Sfmt 4703 Research; 93.397, Cancer Centers Support; 93.398, Cancer Research Manpower; 93.399, Cancer Control, National Institutes of Health, HHS.) Dated: May 12, 2005. LaVerne Y. Stringfield, Director, Office of Federal Advisory Committee Policy. [FR Doc. 05–10071 Filed 5–19–05; 8:45 am] BILLING CODE 4140–01–M DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Cancer Institute; Notice of Meeting Pursuant to section 10(d) of the Federal Advisory Committee Act, as amended (5 U.S.C. Appendix 2), notice is hereby given of the meeting of the National Cancer Advisory Board. The meeting will be open to the public as indicated below, with attendance limited to space available. Individuals who plan to attend and need special assistance, such as sign language interpretation or other reasonable accommodations, should notify the Contact Person listed below in advance of the meeting. A portion of the meeting will be closed to the public in accordance with the provisions set forth in sections 552b(c)(4), and 552b(c)(6), as amended. The grant applications and the discussions could disclose confidential trade secrets or commercial property such as patentable material, and personal information concerning individuals associated with the grant applications, the disclosure of which would constitute a clearly unwarranted invasion of personal privacy. Name of Committee: National Cancer Advisory Board Subcommittee on Planning and Budget. Open: June 6, 2005, 6:30 p.m. to 9 p.m. Agenda: To discuss activities related to the Subcommittee on Planning and Budget. Place: Hyatt Regency Bethesda, One Bethesda Metro Center, Bethesda, MD 20814. Contact Person: Ms. Cherie Nichols, Executive Secretary, National Cancer Institute, National Institutes of Health, 6116 Executive Boulevard, 2nd Floor, Room 205, Bethesda, MD 20892–2590, (301) 496–5515. Name of Committee: National Cancer Advisory Board. Open: June 7, 2005, 8:30 a.m. to 4:30 p.m. Agenda: Program reports and presentations; Business of the Board. Place: National Cancer Institute, 9000 Rockville Pike, Building 31, C Wing, 6th Floor, Conference Room 10, Bethesda, MD 20892. Contact Person: Dr. Paulette S. Gray, Executive Secretary, National Cancer E:\FR\FM\20MYN1.SGM 20MYN1

Agencies

[Federal Register Volume 70, Number 97 (Friday, May 20, 2005)]
[Notices]
[Pages 29334-29336]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 05-10065]


-----------------------------------------------------------------------

DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, DHHS.

ACTION: Notice.

-----------------------------------------------------------------------

SUMMARY: The inventions listed below are owned by an agency of the U.S. 
Government and are available for licensing in the U.S. in accordance 
with 35 U.S.C. 207 to achieve expeditious commercialization of results 
of federally-funded research and development. Foreign patent 
applications are filed on selected inventions to extend market coverage 
for companies and may also be available for licensing.

ADDRESSES: Licensing information and copies of the U.S. patent 
applications listed below may be obtained by writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, 
Maryland 20852-3804; telephone: 301/496-7057; fax: 301/402-0220. A 
signed Confidential Disclosure Agreement will be required to receive 
copies of the patent applications.

DU145 Camptothecin (CPT)-Resistant Cell Line

Dr. Yves Pommier (NCI)
DHHS Reference No. E-159-2005/0--Research Tool
Licensing Contact: John Stansberry; 301/435-5236; stansbej@mail.nih.gov

    Drug resistance is a major limitation of chemotherapy. 
Understanding how drug resistance develops may lead to more effective 
treatments. This invention describes the DU145 Camptothecin (CPT)-
resistant prostate cancer cell line that can be used to study 
mechanisms of drug resistance. For more details see Pommier et al., 
Cancer Research 61, 1964-1969, March 1, 2001.

Mammary Gland Differentiation by 2-Methoxyestradiol

Jeffrey E. Green et al. (NCI)
DHHS Ref. No. E-069-2005/0-US-01
Licensing Contact: Thomas P. Clouse; 301/435-4076; clouset@mail.nih.gov

    This invention is based on the discovery that administration of 2-
Methoxyestradiol (2-ME2) to female mice at various developmental stages 
will result in the differentiation of mammary epithelial cells to form 
rudimentary alveolar structures and to produce milk proteins. This 
effect has also been demonstrated in an in vitro experimental system. 
Since 2-ME2 is highly expressed during late stages of human pregnancy 
and pregnancy is known to reduce the risk of human bresat cancer, 
possibly due to differentiating effects on the mammary gland, 2ME2 may 
be developed into a preventive agent against breast cancer in women. 
Additionally, 2-ME2 may be useful in augmenting mammary gland 
differentiation and milk production under circumstances where normal 
differentiation is compromised.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Methods for Detecting Progression of Low Grade Cervical Dysplasia

Thomas Ried et al. (NCI)
DHHS Reference No. E-041-2005/0-US-01
Licensing Contact: Thomas P. Clouse; 301/435-4076; clouset@mail.nih.gov

    This invention describes a test that can be applied to Pap smears 
to differentiate low-grade dysplastic lesions that are likely to 
progress to higher-grade dysplasia and cervical cancer from those that 
are likely to regress. The differentiating factor is the presence of 
genetic gain on the long arm of chromosome 3. The inventors have shown 
that low grade Pap smears that progress already exhibit extra copies of 
3q, while those that do not show the 3q gain spontaneously regress.
    Around 10-15% of the 3 million Pap smears with low-grade dysplasia 
each year in the United States progress to higher grade lesions. 
Currently, HPV testing is used to stratify these low grade disease Pap 
smears, but as the majority of these Pap smears are already HPV 
infected, the test has very low specificity. The instant 3q test, which 
targets the human telomerase gene, TERC, is a significant improvement 
in sensitivity and specificity over the current methods used for the 
detection of progressing versus regressing lesions.

Antibodies to Rheb, a Ras-Related Protein

Geoffrey J. Clark and Michele Vos (NCI)
DHHS Reference No. E-351-2004--Research Tool.
Licensing Contact: Mojdeh Bahar; 301/435-2950; baharm@mail.nih.gov

    The invention relates to polyclonal antibodies that recognize the 
protein Rheb, a key player in protein biosynthesis. Rheb is a small 
GTP-binding protein that is structurally related to the oncoprotein 
Ras, but Rheb does not activate the same pathways as Ras. Instead, Rheb 
binds to the tumor suppressor TSC2 (Tuberin) and causes activation of 
the S6 kinase in a TOR (Target of Rapamycin) dependent manner. Rheb 
likely plays roles in the response to insulin and the development of 
human tumors. Thus, the antibodies could provide useful reagents to 
investigate the functions of Rheb in these and other biological 
processes.

[[Page 29335]]

    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.

Methods of Reducing the Activity and Concentration of an Eph Receptor 
Tyrosine Kinase

Jennifer Isaacs and Leonard Neckers (NCI)
U.S. Provisional Application No. 60/591,986 filed 29 Jul 2004 (DHHS 
Reference No. E-245-2004/0-US-01)
Licensing Contact: George Pipia; 301/435-5560; pipiag@mail.nih.gov

    The Eph receptors comprise a family of 14 members and as such, they 
carry out diverse functions, including embryonic patterning, migration, 
and the formation of neural networks. Recently, it was discovered that 
a subset of these proteins play an integral role in the formation of 
blood vessels, or angiogenesis, which is a process essential to tumor 
development. In fact, several of these proteins have the capacity to 
transform normal cells, when overexpressed. We have discovered that the 
HSP90 inhibitor 17-Allylamino-17-demethoxygeldanamycin (17-AAG) 
effectively downregulates the level of several angiogenic Eph receptors 
and impairs their oncogenic signaling. This suggests that it maybe 
possible treat cancers overexpressing these oncogenes, by selectively 
inhibiting HSP90 with 17-AAG and its derivatives.

Retinal Pigment Epithelial Cells Immortalized with TERT and Expressing 
the Adenoviral E1A Oncoprotein

Karen Vousden et al. (NCI)
DHHS Reference No. E-135-2004/0--Research Tool
Licensing Contact: Thomas P. Clouse; 301/435-4076; clouset@mail.nih.gov

    This invention describes human retinal pigment epithelial cells 
immortalized with telomerase reverse transcriptase (TERT). Some of 
these cells express the adenoviral E1A oncoprotein, while others do 
not. The E1A expressing cells serve as a model for cancerous cells. 
Those that do not express E1A behave like normal cells. As such these 
immortalized cells can be used to compare the behavior of normal and 
cancer cells in vitro.

Analogs of Thalidomide as Potential Angiogenesis Inhibitors

William D. Figg, Erin Lepper (NCI)
U.S. Provisional Application No. 60/486,515 filed 11 Jul 2003 (DHHS 
Reference No. E-272-2003/0-US-01); PCT Application No. PCT/US04/22242 
filed 09 Jul 2004 (DHHS Reference No. E-272-2003/0-PCT-02)
Licensing Contact: Jesse Kindra; 301/435-5559; kindraj@mail.nih.gov

    The present disclosure relates to anti-angiogenesis compositions 
and methods, and particularly thalidomide analogs that actively inhibit 
angiogenesis in humans and animals.
    Angiogenesis is the formation of new blood vessels from pre-
existing vessels. Angiogenesis is prominent in solid tumor formation 
and metastasis. A tumor requires formation of a network of blood 
vessels to sustain the nutrient and oxygen supply for continued growth. 
Some tumors in which angiogenesis is important include most solid 
tumors and benign tumors, such as acoustic neuroma, neurofibroma, 
trachoma, and pyogenic granulomas. Prevention of angiogenesis could 
halt the growth of these tumors and the resultant damage due to the 
presence of the tumor.
    The subject application discloses active thalidomide analogs that 
exhibit enhanced potency in the inhibition of undesirable angiogenesis, 
and methods for using these compounds to treat angiogenesis and solid 
tumors. In particular, the presently disclosed method provides for 
inhibiting unwanted angiogenesis in a human or animal by administering 
to the human or animal with the undesired angiogenesis a composition 
comprising an effective amount of the active thalidomide analogs. 
According to a more specific aspect, the method involves inhibiting 
angiogenesis by exposing a mass having the undesirable angiogenesis to 
an angiogenesis inhibiting amount of one or more compounds, or 
pharmaceutically acceptable salts of such compounds.

Mycolactone and Related Compounds

Pamela L. Small and Kathleen M. George (NIAID)
U.S. Patent 6,680,055 issued 20 Jan 2004 (DHHS Reference No. E-199-
1999/0-US-06)
Licensing Contact: John Stansberry; 301/435-5236; stansbej@mail.nih.gov

    This application describes and claims novel pharmocoactive 
compounds which belong to the class of compounds known as polyketide 
macrolides. These compounds have been isolated from M. ulcerans the 
causative agent of buruli ulcers. Early work with these compounds 
suggests that the principle compound, mycolactone, or mixtures of 
mycolactone with other isolated polyketide macrolides or other agents 
may be useful in treating cancer or suppressing an inflammatory 
response.
    In addition to the novel polyketide macrolide compounds the 
application also describes compositions derived from a non-virulent 
strain of M. ulcerans. These compositions may be useful in inducing an 
immune response (vaccines) which could be useful in providing subjects 
with resistance to the development of buruli ulcers. Antibodies against 
mycolactone are being developed. These antibodies could be used for 
diagnostic purposes.
    Some early publications which describe this work are KM George et 
al. Science 283(5403): 854-7 (Feb. 5, 1999) and KM George et al. 
Infect. Immun. 66(2): 587-93 (Feb. 1998). More recently, novel 
mycolactones have been isolated and characterized from Australian 
isolates of M. ulcerans (Judd et al. Organic Lett. 6: 4901-4904 (2004)) 
as well as from the frog pathogen M. liflandii (Mve-Obiang, A. et al. 
Infect. Immun. (In Press)).

Spatial and Temporal Control of Gene Expression Using a Heat Shock 
Protein Promoter in Combination with Local Heat

Chrit T. Moonen (ORS)
U.S. Patent Application No. 10/864,102 filed 09 Jun 2004, claiming 
priority to 15 Aug 1996 (DHHS Reference No. E-235-1995/0-US-09); 
Foreign rights available
Licensing Contact: George Pipia; 301/435-5560; pipiag@mail.nih.gov

    In many instances, it is desirable to express exogenous genes only 
in certain tissues, and/or at will at certain times, and/or only to a 
certain degree. However, current gene transfer and exogenous gene 
expression protocols do not provide adequate means of simultaneously 
controlling which cells in a heterogeneous population are transformed 
and when, where, and to what degree the transferred genes are 
expressed. The invention provides methods for using local heat to 
control gene expression. The heat shock protein (hsp) gene promoter is 
recombined with a selected therapeutic gene and expressed in selected 
cells. Local controlled heating is used to activate the hsp promoter, 
for example by using focused ultrasound controlled by MRI.
    In addition to licensing, the technology is available for further 
development through collaborative research opportunities with the 
inventors.


[[Page 29336]]


    Dated: May 11, 2005.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 05-10065 Filed 5-19-05; 8:45 am]
BILLING CODE 4140-01-P

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